The dermatologist's interest in porphyrin metabolism has been concerned mainly with abnormal formation and excretion of porphyrin in rare cases of chronic or congenital sensitivity to light.1 It was first thought that hematoporphyrin was the porphyrin which accounted for the clinical symptoms of hydroa aestivale, as it could be shown that hematoporphyrin was possessed of photosensitizing powers when injected experimentally into animals2 and into human beings.3 Later Fischer4 proved that hematoporphyrin, which is readily prepared in the laboratory from blood, does not appear to play any important role in porphyrin metabolism in nature. In a long series of investigations in the case of congenital porphyria of Petry, Fischer was able to show that the excreted porphyrins differed fundamentally from hematoporphyrin in the melting point of the esters and in a greater number of carboxyl groups in the molecule. These porphyrins were labeled uroporphyrin and coproporphyrin. Coproporphyrin,